Painless penile papule

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Painless penile papule

J Fam Pract. 2015 March;64(3):185-186,188

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References

1. Goldsmith, Lowell, Fischer B. Syphilis. Rochester, NY: VisualDx. Available at: http://www.visualdx.com/. Updated January 19, 2015. Accessed February 13, 2015.

2. Allen C, Woo SB. Aphthous Stomatitis. Rochester, NY: VisualDx. Available at: http://www.visualdx.com/. Updated August 21, 2013. Accessed February 13, 2015.

3. Zetola NM, Klausner JD. Syphilis and HIV Infection: an update. Clin Infect Dis. 2007:44:1222-1228.

4. Marra CM. Syphilis and human immunodeficiency virus infection. Semin Neurol. 1992;12:43-50.

5. Rompalo AM, Lawlor J, Seaman P, et al. Modification of syphilitic genital ulcer manifestations by coexistent HIV infection. Sex Transm Dis. 2001;28:448-454.

6. Schöfer H, Imhof M, Thoma-Greber E, et al. Active syphilis in HIV infection: a multicentre retrospective survey. The German AIDS Study Group (GASG). Genitourin Med. 1996;72:176-181.

7. James WD, Berger T, Elston D. Andrew’s Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, PA: Saunders; 2011.

8. Lynn WA, Lightman S. Syphilis and HIV: a dangerous combination. Lancet Infect Dis. 2004;4:456-466.

9. Musher DM. Syphilis, neurosyphilis, penicillin, and AIDS. J Infect Dis. 1991;163:1201-1206.

10. Marra CM, Maxwell CL, Smith SL, et al. Cerebrospinal fluid abnormalities in patients with syphilis: association with clinical and laboratory features. J Infect Dis. 2004;189:369-376.

11. Sadiq ST, McSorley J, Copas AJ, et al. The effects of early syphilis on CD4 counts and HIV-1 RNA viral loads in blood and semen. Sex Transm Infect. 2005;81:380-385.

12. Kofoed K, Gerstoft J, Mathiesen LR, et al. Syphilis and human immunodeficiency virus (HIV)-1 coinfection: influence on CD4 T-cell count, HIV-1 viral load, and treatment response. Sex Transm Dis. 2006;33:143-148.

13. Dyer JR, Eron JJ, Hoffman IF, et al. Association of CD4 cell depletion and elevated blood and seminal plasma human immunodeficiency virus type 1 (HIV-1) RNA concentrations with genital ulcer disease in HIV-1-infected men in Malawi. J Infect Dis. 1998;177:224-227.

14. Buchacz K, Patel P, Taylor M, et al. Syphilis increases HIV viral load and decreases CD4 cell counts in HIV-infected patients with new syphilis infections. AIDS. 2004;18:2075-2079.

15. Palacios R, Navarro F, Narankiewicz D, et al. Liver involvement in HIV-infected patients with early syphilis. Int J STD AIDS. 2013;24:31-33.

16. Centers for Disease Control and Prevention. 2010 STD Treatment Guidelines. Centers for Disease Control and Prevention Web site. Available at: http://www.cdc.gov/std/treatment/2010/genital-ulcers.htm#a5. Accessed February 4, 2015.

How syphilis affects HIV, and vice versa

HIV infection has been known to alter the natural history and presentation of syphilis, and syphilis may also impact the course and evaluation of HIV infection.³ Syphilis and other infections that lead to genital ulcers increase an individual’s propensity to acquire HIV due to the loss of the barrier function of the epithelial membrane and the production of cytokines stimulated by treponemal lipoproteins.⁴ This facilitates transmission of the virus.

Syphilis may have an atypical clinical presentation in patients who are also infected with HIV. In the typical clinical presentation of primary syphilis in an immunocompetent patient, an indolent papule develops 10 to 90 days after inoculation and subsequently ulcerates into an indurated chancre. Patients with HIV may develop multiple chancres that are larger, deeper, and more ulcerative.^4-6 Approximately one-quarter of these patients present with lesions of both primary and secondary syphilis at the time of diagnosis.⁵ However, our patient presented with a solitary painless indurated papule after years of stable and well-controlled HIV infection; this suggests that cutaneous manifestations of syphilis may have atypical clinical presentations in patients who are also infected with HIV.^5,6

What you’ll see in the secondary stage

In immunocompetent patients, secondary syphilis is characterized by fever, malaise, lymphadenopathy, moth-eaten alopecia, focal neurologic findings, condyloma lata, mucocutaneous aphthae, and a generalized papulosquamous eruption.⁷ After 3 to
12 weeks, the secondary infection spontaneously disappears and leads into the latency period, which may last years. Thirty percent of untreated patients progress from latent to tertiary syphilis.⁷ During this stage, treponemes invade the central nervous system, heart, bone, and skin, triggering vigorous host cellular immune responses and delayed-type hypersensitivity reactions.

When complicated by HIV, secondary syphilis may present along a more aggressive course, with early neurologic and ophthalmologic involvement.⁸ Patients coinfected with syphilis and HIV are also more prone to developing neurosyphilis—even after completing penicillin therapy—and a more intensive diagnostic evaluation should be considered for such patients.⁹ Higher protein levels and lower glucose levels in the cerebrospinal fluid are also reported in HIV-infected patients with syphilis,¹⁰ likely due to the weakened host immune response.